The regeneration of pancreatic β-cells has become an important factor for the purpose in curing Diabetes mellitus. The concept that β-cell mass is static has changed and now we know that β-cells are dynamic and to certain extent can compensate for the loss of blood glucose and retain their ability to respond to changes in blood glucose by their ability to maintain glucose homeostasis. These studies are based on the experimental animal models. In continuation with the same efforts have been made to search for the factors that lead to direct differentiation of β-cells from precursor cells and those responsible for proliferation of existing β-cells in the residual β-cell mass in the diabetic individual. The aims of these efforts are to find out novel molecules to control and cure diabetes by natural products.
Rat AR42J is derived from a chemically induced pancreatic tumor having exocrine origin and has the feature of pluri-potency of the common precursor cell of the pancreas. It has been reported that amylase secreting AR42J cells convert themselves into insulin secreting cells in the presence of hepatocyte growth factor and or in the presence of betacellulin and activin A. Reference may be made to a publication wherein rat AR42J cells were derived from a chemically induced pancreatic tumor having exocrine origin and have the feature of pluri-potency of the common precursor cell of the pancreas (Mashima H, Ohnishi H, Wakabayashi K. Mine T., Miyagawa J, Hanahusa Ta, Seno M, Yamada H, Kojima I, Betacellulin and activin A coordinately convert amylase-secreting pancreatic AR42J cells in to insulin-secreting cells, J. Clin Invest 97:1647–1654, 1996; Mashima H, Yamada S, Tajima T., Seno M, Yamada H, Takeda J and Kojima I. Genes Expressed During the differentiating of Pancreatic AR42J cells into insulin-secreting cells, Diabetes, 48, p 304–309, 1999).